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Glioma cell activation by Alzheimer's peptide Abeta1-42, alpha1-antichymotrypsin, and their mixture.

Sun, Yongxin LU ; Wright, H T and Janciauskiene, Sabina LU (2002) In Cellular and Molecular Life Sciences1997-01-01+01:00 59(10). p.43-1734
Abstract
We compared the effects of Alzheimer’s peptide

(Ab1–42), a1-antichymotrypsin (ACT) and an ACT/Ab1–42

mixture on human glioma DK-MG cells. The solution of

Ab (5 mM) formed by 2-h incubation at room temperature

induced tumour necrosis factor-a (TNF-a) and interleukin

(IL)-6 levels by 55 and 45%, respectively, and increased

gelatinase B activity by 67%, while exposure of

cells to the ACT/Ab1–42 mixture (1:10 molar ratio ACT:

Ab1–42) under the same experimental conditions showed

no effect on IL-6 levels or gelatinase B activity, but

strongly induced TNF-a (by 190%), compared to the con-

CMLS, Cell. Mol. Life Sci. 59 (2002) 1734–1743

... (More)
We compared the effects of Alzheimer’s peptide

(Ab1–42), a1-antichymotrypsin (ACT) and an ACT/Ab1–42

mixture on human glioma DK-MG cells. The solution of

Ab (5 mM) formed by 2-h incubation at room temperature

induced tumour necrosis factor-a (TNF-a) and interleukin

(IL)-6 levels by 55 and 45%, respectively, and increased

gelatinase B activity by 67%, while exposure of

cells to the ACT/Ab1–42 mixture (1:10 molar ratio ACT:

Ab1–42) under the same experimental conditions showed

no effect on IL-6 levels or gelatinase B activity, but

strongly induced TNF-a (by 190%), compared to the con-

CMLS, Cell. Mol. Life Sci. 59 (2002) 1734–1743

1420-682X/02/101734-11

© Birkhäuser Verlag, Basel, 2002 CMLS Cellular and Molecular Life Sciences

trols. Stimulation of the cells with Ab1–42 alone, but not

with ACT, increased by about 20% low-density lipoprotein

(LDL) uptake and mRNA levels for LDL receptor and

HMG-CoA reductase, while the ACT/Ab1–42 mixture significantly

increased LDL uptake (by 50%), up-regulated

mRNA levels for LDL receptor and HMG-CoA reductase

by 48 and 63%, respectively, and increased lipid accumulation

by about 20-fold. These data suggest a possible new

role for Ab in Alzheimer’s disease through its interaction

with the inflammatory reactant, ACT. (Less)
Please use this url to cite or link to this publication:
@article{18a24388-07ac-40da-8a41-332b2ccc3b74,
  abstract     = {We compared the effects of Alzheimer’s peptide<br/><br>
(Ab1–42), a1-antichymotrypsin (ACT) and an ACT/Ab1–42<br/><br>
mixture on human glioma DK-MG cells. The solution of<br/><br>
Ab (5 mM) formed by 2-h incubation at room temperature<br/><br>
induced tumour necrosis factor-a (TNF-a) and interleukin<br/><br>
(IL)-6 levels by 55 and 45%, respectively, and increased<br/><br>
gelatinase B activity by 67%, while exposure of<br/><br>
cells to the ACT/Ab1–42 mixture (1:10 molar ratio ACT:<br/><br>
Ab1–42) under the same experimental conditions showed<br/><br>
no effect on IL-6 levels or gelatinase B activity, but<br/><br>
strongly induced TNF-a (by 190%), compared to the con-<br/><br>
CMLS, Cell. Mol. Life Sci. 59 (2002) 1734–1743<br/><br>
1420-682X/02/101734-11<br/><br>
© Birkhäuser Verlag, Basel, 2002 CMLS Cellular and Molecular Life Sciences<br/><br>
trols. Stimulation of the cells with Ab1–42 alone, but not<br/><br>
with ACT, increased by about 20% low-density lipoprotein<br/><br>
(LDL) uptake and mRNA levels for LDL receptor and<br/><br>
HMG-CoA reductase, while the ACT/Ab1–42 mixture significantly<br/><br>
increased LDL uptake (by 50%), up-regulated<br/><br>
mRNA levels for LDL receptor and HMG-CoA reductase<br/><br>
by 48 and 63%, respectively, and increased lipid accumulation<br/><br>
by about 20-fold. These data suggest a possible new<br/><br>
role for Ab in Alzheimer’s disease through its interaction<br/><br>
with the inflammatory reactant, ACT.},
  author       = {Sun, Yongxin and Wright, H T and Janciauskiene, Sabina},
  issn         = {1420-9071},
  keyword      = {Kinetics,Peptide Fragments: chemical synthesis,Human,Interleukin-6: genetics,DNA Primers,DNA,Neoplastic: drug effects,Glioma: physiopathology,Amyloid beta-Protein: pharmacology,Base Sequence,Amyloid beta-Protein: chemical synthesis,Gene Expression Regulation,Neoplasm: biosynthesis,Gelatinase B: metabolism,Peptide Fragments: pharmacology,RNA,Messenger: genetics,Reverse Transcriptase Polymerase Chain Reaction,Support,Non-U.S. Gov't,Thymidine: metabolism,Transcription,Genetic: drug effects,Tumor Cells,Cultured,Tumor Necrosis Factor: genetics,alpha 1-Antichymotrypsin: pharmacology},
  language     = {eng},
  number       = {10},
  pages        = {43--1734},
  publisher    = {Birkhaüser},
  series       = {Cellular and Molecular Life Sciences1997-01-01+01:00},
  title        = {Glioma cell activation by Alzheimer's peptide Abeta1-42, alpha1-antichymotrypsin, and their mixture.},
  url          = {http://dx.doi.org/10.1007/PL00012501},
  volume       = {59},
  year         = {2002},
}